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Biomedical subjects

M Carstensen

Publications and source records attributed to M Carstensen.

11 recordsLinked to original sources
PubMed1994

Input impedance of the lower abdominal aorta in chronically instrumented fetal sheep.

Five fetal sheep (gestational age, 118 to 125 days) were instrumented to measure impedances of the lower abdominal aorta. Four days after surgery, flow and pressure pulses were recorded during control conditions and during infusion of norepinephrine (0.3 to 3 micrograms.min-1.kg-1 body weight) or angiotensin II (0.2 to 3 micrograms.min-1.kg-1). The protocol was repeated after injection of hexamethonium (10 mg.kg-1). Moduli and phases of impedances for the first ten harmonics were calculated by fast Fourier transformation. During control, input resistance was 4300 +/- 940 dyne.s.cm-5 (mean +/- SD) at a mean blood flow of 13.3 +/- 2.4 cm3.s-1 and pressure of 54,960 +/- 6980 dyne.cm-2. Moduli fell to 50% of input resistance between 2 and 3 Hz and, declining continuously, reached a minimum of 20% near 10 to 12 Hz, then increased slightly to 30% at about 30 Hz. At the first three harmonics, flow was always leading pressure. Infusion of angiotensin or norepinephrine increased impedance moduli significantly. Resistance increase was largest with angiotensin (19,800 +/- 11,370 dyne.s.cm-5), but no difference was detectable between angiotensin and norepinephrine when related to the same increase of input resistance. The position of the minimum seemed to be unchanged at high resistance values, but relative impedance moduli were smaller than during control, and low-frequency phases were significantly more negative. An analog of inertance, compliance, and resistance to steady flow was used to simulate impedances, and the effect of resistance increases on flow waveforms in the fetal abdominal aorta was calculated.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Fetal sheep temperatures in utero during cooling and application of triiodothyronine, norepinephrine, propranolol and suxamethonium.

Fetal sheep (n = 13) were chronically instrumented to measure temperatures in the maternal femoral artery (MAT), the amniotic fluid (AFT), the fetal brown adipose tissue (BFT) and the fetal arterial blood (DAT). Cooling loops were inserted into the amniotic cavity. In 4 fetuses osmotic minipumps delivering triiodothyronine (T3) were implanted subcutaneously. One to seven days after surgery the following results were obtained: 1) During control DAT was 0.59 +/- 0.2 degrees C (SD), BFT 0.60 +/- 0.24 degrees C and AFT 0.38 +/- 0.31 degrees C higher than MAT. T3 levels in treated fetuses were 3.4 +/- 1.5 micrograms/l. 2) Infusion of norepinephrine (NE) (5.2 +/- 0.9 micrograms/min per kg fetal body weight) with phentolamine (26.1 +/- 4.3 micrograms/min per kg) into a fetal vein did not change temperatures. 3) During cooling (-53 +/- 15 W) MAT decreased 0.45 +/- 0.3 degrees C, DAT 1.9 +/- 0.39 degrees C, BFT 1.61 +/- 0.52 degrees C and AFT 4.2 +/- 1.8 degrees C. 4) The amniotic fluid was cooled until steady state temperatures were achieved. Then propranolol (26.1 +/- 4.3 micrograms/min per kg) or suxamethonium (3 +/- 1 mg/kg) were introduced into the fetal vein. No consistent and significant changes of temperatures could be detected. It is concluded that 1) lowering the fetal core temperature by 1.6 - 1.9 degrees C and its ambient temperature (AFT) by 4.2 degrees C does not induce shivering or non-shivering thermogenesis suppressible by pharmacologic agents, 2) thermogenesis in fetal brown adipose tissue cannot be induced by NE (with or without supplemention of T3).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

[Prenatal diagnosis and therapy of hemolytic disease of the newborn].

From 1966 to 1983 a total of 586 intra-uterine fetal transfusions on 268 fetuses suffering from severe Rh-erythroblastosis were performed at the Hamburg university hospital. 149 (56%) fetuses survived. 29% of 268 fetuses exhibited ascitic fluid at the beginning of therapy. The survival rate improved to 63% in the last five years. The diagnostic and therapeutic procedures are explained in detail. The amniotic fluid analysis has been improved. In addition to Rh-antibodies, it is important to detect other blood group antibodies such as anti-Jk(a) and anti-Fy(a), that can diminish the survival rate of the donor erythrocytes in the fetus.

Amniotic Fluid↗
PubMed1981

Congenital malformation syndromes and elevation of amniotic fluid alpha-fetoprotein.

Fetal malformations may introduce complications of maternal pregnancy. A polyhydramnios represents one such complication during pregnancy. We want to report five abnormal pregnancies which were marked by acute polyhydramnios and/or premature labor due to an amniotic band syndrome associated with cerebral herniation in two cases, malignant oral teratoma in one case, bilateral cystic hygromas associated with generalized fetal hydrops in one case, and multiple internal malformations in one case alpha-fetoprotein (AFP) values between the 25th and 34th week of gestation were elevated 3.5 to 44 times the normal median value. Since all fetuses showed severe malformations incompatible with life our observations indicate the necessity to determine AFP in cases of acute polyhydramnios independent of the week of gestation. Conversely, elevated AFP levels in amniotic fluid obtained during prenatal diagnosis in the 16th week of gestation may also suggest rare fetal malformations outlined above.

Amniotic Fluid↗
PubMed1977

Evidence for a specific transport of D-hexoses across the human term placenta in vitro.

Isolated cotylidons of human term placentas are perfused artificially on the fetal and maternal side. The relative transfer rates of radioactive labelled D-glucose, L-glucose, D-mannose and D-mannitol across the placenta are measured and the inhibition of these transports by phloretin is studied: 1. Transfer rates of D-glucose and D-mannose exceed that of L-glucose about 1.5-4 times. 2. Phloretin (10(-3) mol/l) decreases the transports of D-hexoses, whereas the transport of L-GLUCOSE REMAINS UNAFFECTED. 3. If the concentration of D-glucose is increased, the transport of D-mannose is inhibited competitively. 4. L-glucose and D-mannitol equal in transfer rates. These results show, that D-hexoses cross the human placenta by a specific carrier and by simple diffusion.

Biological Transport, Active↗